Unilateral damage to visual cortex of the parietal or occipital lobe can cause the patient to be unaware of contralesional visual information due to either hemispatial neglect or hemianopia. It is now known that both neglect and hemianopia result from the disruption of a dynamic interaction between cortical visual pathways and more phylogenetically primitive visual pathways to the midbrain. We consider the therapeutic implications of these cortical-subcortical interactions in the rehabilitation of hemianopia. We start with the pheonmenon of "blindsight", in which patients with hemianopia can be shown, by implicit measures of visual detection or discrimination, to process visual information without conscious awareness. Some variants of blindsight have been postulated to recruit subcortical processes, while others may reflect compensatory optimisation of processing of spared visual cortex. Both mechanisms may offer opportunities for innovative strategies for rehabilitation of visual field defects. We relate the neural mechanisms that have been proposed to underlie blindsight to those that have been suggested to underlie the recovery of visual function after rehabilitation. It is suggested that the similarity and overlap of the neural processes supporting blindsight and recovery of visual function might provide insights for effective rehabilitation strategies for restoring visual functions.